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An influx of Ca 2+ are resulted due to the affinity of glutamate to N-methyl-d-aspartate (NMDA) receptors, which triggers a cyclic guanosine monophosphate (cGMP)-mediated pathway terminating in protein kinase C (PKC) activation, resulting to decreasing magnesium blockage of NMDA channels and elevating Ca 2+ influx and excitotoxicity [63]

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